Lactic acidosis has long been recognized as a nutritional disease that often occurs in ruminants following an extra large intake of readily fermentable carbohydrate. Traditionally, lactic acidosis occurred when cattle accidently gained access to the farmer's grain fields or grain supply. Today with the advent of high concentrate rations for cattle, lactic acidosis occurs frequently in high producing dairy cows that are placed on high concentrate diets too quickly following initiation of lactation; in feedlot cattle that are rushed too quickly onto high concentrate rations and more subtly in feedlot cattle that are adapted to high concentrate consumption but experience changes in ration or feeding pattern.
In particular, lactic acidosis is a serious problem in cattle during the first few weeks in the feedlot because of the stress due to starvation from shipping and conversion from a roughage to a concentrate diet. Cattle normally consume 10-12 meals per day which allows rumen microbes to thrive. When no feed is ingested for a prolonged period, such as when cattle are shipped to the feedlot, most protozoa and many types of rumen bacteria perish. The lactate producer Streptococcus bovis, however, survives starvation better than most rumen microbes so that starvation increases the relative number of Streptococcus bovis. Most bacteria in the rumen are gram negative and are involved in the conversion of dietary carbohydrates to volatile fatty acids. Streptococcus bovis on the other hand is a gram positive rumen microorganism that converts readily fermentable carbohydrates to DL-lactic acid. Normally Streptococcus bovis does not play a predominant role in rumen fermentation and lactic acid is a minor product of rumen fermentation, however, when ruminants not adapted to high starch ration consume large quantities of readily fermentable carbohydrate Streptococcus bovis multiplies rapidly often outgrowing all other rumen microorganisms, and produces great quantities of DL-lactic acid. The lactic acid lowers rumen fluid pH which prevents normal fermentation by inhibiting other rumen microorganisms and eventually enables lactobacillus, another lactic acid producer, to establish itself in the rumen. The large quantities of DL-lactic acid produced in the rumen are absorbed. L-lactic acid is metabolized by the animal but D-lactic acid accumulates in the blood causing a depletion of the alkali reserve and a shift in blood pH which can cause death.
Lactic acidosis is a major problem in feedlot cattle. Lactic acidosis causes a significant loss in animal production even when the animal survives because of conditions associated directly or indirectly with the disease. These conditions include anorexia, rumen disfunction, diarrhea, weight loss, founder and rumenitis. Rumenitis, an ulceration of the ruminal wall, allows rumen microorganisms especially Spherophorus necrophorus to gain access to the portal circulatory system. These microbes are removed by the liver where they cause liver abscesses which reduce weight gain and feed efficiency. In addition, the abscessed livers are condemned at slaughter resulting in further economic losses. Thus lactic acidosis reduces animal productivity not only through death losses but also through reduced performance caused by poor animal health. The only known method of preventing lactic acidosis is to slowly adapt cattle to a high energy ration. The time required to adapt cattle is not well defined, however, most cattle feeders allow at least 3 to 4 weeks. During this time most feeders gradually switch from a ration having a concentrate to roughage ratio of 1:3 to a ration having a ratio of 3:1 or higher. One of the problems with this approach is that the low energy rations used initially do not produce sufficient energy for restoration of animal health and disease resistance following the stress of shipping to the feedlot. In addition, slow adaptation does not allow for rapid adjustment to fattening (high energy) rations which cost the cattle feeder time and money. None of the antibiotics presently available for use in ruminants control lactic acidosis.
It is an aspect of this invention that the antibiotics employed in the treatment of lactic acidosis be effective against the microorganism Streptococcus bovis, however, all antibiotics effective against Streptococcus bovis may not be effective against lactic acidosis. Should the antibiotic destroy significant numbers of rumen microorganisms beyond Streptococcus bovis then rumen functions will effectively cease and metabolism of ingested feed will also cease resulting in serious nutritive disorders. Normal rumen bacteria consists primarily of gram negative bacteria. Thus it is also an aspect of this invention that the antibiotic have a spectrum substantially limited to gram positive bacteria and excluding the majority of the normal rumen bacteria in order that the normal rumen microorganisms not be effected so that normal rumen function continues while the antibiotic is being administered to the ruminant.